CD4 helper T cell

AIDS (acquired immunodeficiency syndrome) is the final stage of disease caused by infection with HIV. In this stage, the vims infection has severely affected the immune system, causing a depletion of CD4+ T-helper cells. AIDS is characterized by the manifestation of typical diseases caused by opportunistic infections (Pneumocystis carinii pneumonia, CMV retinitis, candidiasis of the esophagus, cerebral toxoplasmosis), neurological manifestations, cachexia, or certain tumors (Kaposi sarcoma of the skin, B-cell lymphoma). 

Lymphocytes, the effector cells of the acquired immune system, include morphologically indistinguishable T and B cells, the former divided into CD4+ T helper cells and CD8+ cytotoxic T cells. Since the functions of those cell subsets differ so drastically, it became important to develop tools to distinguish them from each other. Efforts to identify cell subsets according to their expression of different surface antigens have been successful, including various Cluster of Determination (CD) markers (Table 23.1). In addition, cross-reactive monoclonal antibodies, and subsequently developed species-specific polyclonal and monoclonal antibodies towards the major histocompatibility complex (MHC) have been used to label cells in circulation and in tissue sections (Table 23.1). 

B cells are produced by the bone marrow. In response to activation of CD4+ T helper cells (see below), B cells proliferate and produce antibodies. (The term CD stands for cluster of differentiation. They are proteins coating cell surfaces. Altogether, there are more than 160 different types of CDs.) The antibodies produced by B cells circulate in the bloodstream and bind to antigens. Once bound, other cells are in turn activated to destroy the antigens. 

IL-2 is possibly the most-studied interleukin. It is also called T cell growth factor. IL-2 is a ISkDa glycoprotein produced by CD4+ T helper cells. It has 133 amino acids. There are four helical regions and a short )3-sheet section (Fig. 4.7). 

Hansen G, Mclntire JJ, Yeung VP, et al CD4+ T-helper cells engineered to produce latent TGF-(Jj reverse allergen-induced airway hyperreactivity and inflammation. J Clin Invest 2000 105 61-70. 

AIDS represents the classic example of immunodeficiency disease caused by extrinsic factors, in this instance the human immunodeficiency virus (HIV). This virus exhibits a strong tropism for CD4 T helper cells these become depleted, giving rise to increased frequency of opportunistic infections and malignancies in infected individuals. AIDS is also characterized by an imbalance in THl and TH2 cells, and the ratios of cells and their functions are skewed toward TH2. This results in hypergammaglobulinemia, loss of cytotoxic lymphocyte activity, and delayed hypersensitivity. 

Spielings E, Vermeulen CJ, Vogt MH, Doemer LE, et al. 2003. Identification of HLA class II restricted H-Y-specific T-helper epitope evoking CD4+ T-helper cells in H-Y-mismatched transplantation. Lancet. 362 610-615. 

Williams, D.L., Asahi, H., Botkin, D.J. and Stadecker, M.J. (2001) Schistosome infection stimulates host CD4(+)T helper cell and B-cell responses againsta novel egg antigen, thioredoxin peroxidase. Infection and Immunity 69, 1 1 34-11 41. 

As described above, peptide epitopes bound to MHC class I or II molecules are able to stimulate CD8+ and CD4+ T cells, respectively. Both CD4+ T-helper cells and CD8+ CTLs are critical to protective immunity and to vaccine efficacy. CD4+ T-helper cells play an important role in the development of memory B-cell (antibody) and memory CTL (cytotoxic T-cell) responses. CD4+ T-helper cells are also active against pathogens on their own. Therefore, CD4+ T-helper cells have been called the conductors of the immune system orchestra (14). CD8+ CTLs are able to directly kill infected target cells and thus are critical in the containment of... 

To counter the low success rate of B-cell epitope prediction, MHC class II epitopes for CD4+ T cells may be emphasized when antibody response is key in vaccine design. CD4+ T-helper cells are critical to induce the activation of B cells that produce antibodies. B-cell antigens that contain significant MHC class II epitopes may outperform B-cell antigens without cognate help. An identified T-cell epitope may sometimes contain a B-cell epitope. In addition, B-cell epitopes may colocalize near or overlap MHC class II epitopes (32, 33). 

Several studies have shown that tumor-specific CD4 T cells play a central role in initiating and maintaining protective immune responses against cancer, and the lack of these T cells in any vaccine strategy could be the cause for weak and transitory immune responses [285,291,326,327]. There are, however, few effective methods for identifying MHC class Il-restricted tumor antigens that can stimulate CD4 T helper cells, and in addition to that, the... 

Stimulation of B cells to proliferate and differentiate into memory and plasma cells depends on epitope binding to epitope-specific receptors on CD4+ T-helper cells. Transmembrane signaling then requires the coreceptor protein CD3. Binding of the T-cell receptor to the antigen-presenting B cell occurs via the TcR that interacts with... 

Jonuleit H, Schmitt E, Kakirman H, Stassen M, Knop J, Enk AH Infectious tolerance human CD25(+) regulatory T cells convey suppressor activity to conventional CD4(+) T helper cells. J Exp Med 2002 196 255-260. 

By GD 100, there is a distinct T cell differentiation toward CD2, CD3, and CD4 (T-helper cells) antigen expression. B cells have formed a thin line on the outer aspect of the T cell cortical region. Further B cell differentiation is apparent by CD35 (activated B cells) and CD138 (plasma cells) immune reactivity. The appearance of these cells correlates well with the presence of serum immunoglobulins such as IgM. 

Adaptive immune response develops in response to infection, protects against specific pathogens and develops memory inducing lifelong immunity to re-infection by the same pathogen. Adaptive immune response relies on T lymphocytes and B lymphocytes that all secrete cytokines T cells fall into two classes (1) CD4+T helper cells (Th) that develop and... 

Zhejiang Province, China, children N = 73) 3-6 years old PbB range 3—40 pg/ dl Abundance of selected lymphocyte cell types cytotoxic CD8 T cells, CD3 T cells, CD4 /CD8 T helper cells. CD4 T helper cells, B cells With children s PbBs alO pg/dl, lower abundance of CD3 /CD4 and CD4V CD8 and higher % of CD3VCD8 cells Zhao et al. (2004)... 

Analysis of BAL fluids might provide useful supportive data in the diagnosis of allergic alveolitis and usually reveals intense lymphocytosis of predominantly CD8-h T-suppressor cells (Patel et al. 2001). On the contrary, in sarcoidosis, BAL fluid usually demonstrates CD4+ T-helper cell lymphocytosis (Sharma and Fujimura 1995). 

LAB as cytokine delivery vector It is now recognized that regulatory T cells (Treg) play a central role in gut homeostasis by maintaining immune tolerance and controlling inflammation. Indeed, a h) per-activation of CD4(+) T helper cells leads to an excessive and uncontrolled immune response, such as in the case of CD and UC, which have been putatively described to possess the Th 1/Th 17 and Th2 phenotype respectively (Ruddy et al. 2004 Leon et al. 2006). Several studies have shown that certain profiles of cytokines, which are produced by immune cells and involved in T cell activation and differentiation, have been directly associated with IBD. In particular, cytokines such as IFTSf- y, IL-17, IL-22, and IL-23 are dysregulated in IBD (Sarra et al. 2010). 

---